Scientists at the University of California – Los Angeles believe their new research shows why current Alzheimer’s drugs are often ineffective in stopping the progression of the disease.
Finding an effective medication for Alzheimer’s ranks high on the agendas of medical professionals and policymakers as the number of people living with Alzheimer’s disease is projected to soar from 5 million to 13.8 million by 2050.
Current medications do not treat Alzheimer’s or stop it from progressing; they only temporarily lessen symptoms, such as memory loss and confusion.
Researchers determined that existing Alzheimer’s drugs aim to reduce the amyloid plaques — sticky deposits that build up in the brain — that are a visual trademark of the disease. The plaques are made of long fibers of a protein called amyloid beta.
Recent studies, however, suggest that the real culprit behind Alzheimer’s may be small amyloid beta clumps called oligomers that appear in the brain years before plaques develop.
In unraveling oligomers’ molecular structure, UCLA scientists discovered that amyloid beta has a vastly different organization in oligomers than in amyloid plaques. Their finding could shed light on why Alzheimer’s drugs designed to seek out amyloid plaques produce zero effect on oligomers.
The UCLA study, published in the Journal of Biological Chemistry, suggests that recent experimental Alzheimer’s drugs failed in clinical trials because they zero in on plaques and do not work on oligomers.
Future studies on oligomers will help speed the development of new drugs specifically aiming at amyloid beta oligomers.